4. Features Primary dention Permanent dention
Gingival colour More reddish Coral pink
contour Free gingival margin-
rounded
Gingival margin-
knife edge
Consistency Flabby due to less CT
density and lack of
organized collagen fiber
bundles
Firm and resilient
Surface texture No Stippling
`Mostly seen by age of 6
years
Stippling present
6. Comparison of normal periodontium in children & adults
Gingival features Primary dentition Factors responsible Permanent dentition
Marginal gingiva Thicker &
rounder around
primary teeth
Due to constricted neck
of p.molar such as
cervical bulge and the
underlying constriction
at cemento-enamel
junction
immature.collagen
fibers (space) increase
b.v
Thin & knife edge margin .
Attached gingiva Flaccid , less dense
, red &
leas stippled .
Wider than p varies
anterioposteriorly
3 to 6mm.
Due to lncreas
connective tissue
density, well epithelium
layer with greater
vascularity.b.v
Firm & resilient attached
gingiva .
central portion of interdental
papilla is stippled , but
marginal borders are smooth .
7. Inter-dental
gingival
Saddle areas are
present resulting in
a well keratinized
interdental
surface.
Because of
interdental
spacing.
With no contact
points
Can be pyramidal or "
col" shape non-
keratinized area
occupies the gingival
embrasure.
8. Gingival sulcular
depth
Shallower in the
primary
dentition.
to , with an
increase in depth
from anterior to
posterior.
Clinically normal
gingival sulcus.
2to3 mm .
Junctional
epithelium
Thicker
compared to
permanent
dentition .
Phenomenon
thought to reduce
the permeability of
epithelium to
bacterial toxins.
10-20 layers thick
coronally and tapers to
1-2 cells apically at
CEJ.
9. Periodontal ligament
-Similar to the adults except
-There are less fibers per unit area ,
Wider , less dense P.L space.
Cementum
-Covering the outer surface of the root
-Its function is to provide attachment to collagen fibers
of the periodontal ligament .
leading to
Leading to
10. Alveolar bone
Radiographically
-lamina dura is prominent ,
-wider PDL space .
- the crests of interdental
bony septa are:
flat
And normally parallel to //
a line drawn between the
CEJ of adjacent teeth.
Bone part which forms and supports the tooth sockets.
CEJ
17. 1-Dental –plaque -induced gingival
diseases
The most common gingivitis.
Dental plaque
cause
without loss of attachment or bone.
gingival
inflammation
19. A. Eruption gingivitis &pericoronitis:
in (6 to 7 year )At the eruption of (D-E-6-7).
1-Temporary and localized form of gingivitis
with difficult eruption, end after the emerge of teeth.
2-Because the gingival margin receives no protection from the
coronal contour of the tooth + accumulation of food debris
+bacteria
Under the gingival operculum of the partial erupting tooth.
Condition of painful +acute inf. can develop pericoronitis
20. Clinical characteristics:
Pericoronitis
Inflammation of gingival
• Covering the partially erupted tooth.
coronal flap becomes inflamed and swollen .
• Enlarged interferes with occlusion , it gets traumatized and
becomes very painful .
20
21. Treatment:
• Debridement and antibiotic therapy.
• In some cases surgical removal of per
coronal flap (operculectomy) may be
necessary.
21
22. B-Exfoliation of primary teeth
Etiology:
The root resorption + tooth mobility
Sharp root end +irritation of the underlying tissue+food impaction
Cause:
• Loss of function and gingival enlargement
• bleeding and discomfort
Treatment:
• Extraction.
22
24. 1- Puberty gingivitis
• In female (conditioning gingival enlargement) end at 18 y
• At the anterior segment
• interdental papillae is Enlarged
marginal gingiva is red bleeding with touch
Etiology: 1- hormonal fluctuation + dental plaque
Cause gingival inflammation.
2- nutrition deficiency.
Treatment:
Improve oral hygiene + remove local irritation + proper nutrition.
If there is no response Gingivectomy.
25. 2- Diabetes mellitus associated
gingivitis
• In diabetic patient :
• Change the insulin level + dental plaque
• + inflammation response
• Cause gingival inflammation
Treatment :
• Improve oral hygiene
• Remove local irritation (plaque and bacterial
deposition)
25
27. • Drug-induced gingival enlargement in children :
• Anti-convulsant agents:
For epileptic children
Ex: - Dilantin - Phenotoin
After few weeks of use cause
• (PIGO)
• Phenytoin induced gingival over growth
27
28. Clinical Feature:
• The growth starts as a painless, beadlike
enlargement of the interdental papilla
• lobulated ,pink +firm
• Doing psedo-pockets
• Depth more than 4m.
• Extends to the facial and Anterior region.
• It may delayed the eruption.
• As the condition progress, may develop into a
periodontal dis. + tissue trauma.
• May interfere with occlusion ,speech,mastication
and aesthetic.
28
29. Treatment modalities
-Change the drug , with consultation with the physician.
-Improve oral hygiene.
- Oral prophylaxis and home care is needed.
daily use of chlohexidine may prevent inflammation.
-Remove local irritation (plaque and bacterial deposition)
-Drugs : Anti histamine + anti biotic +Folic acid vitamin
- If there is no response: gingivectomy
31. . Scorbutic gingivitis
• Associated with vitamin C deficiency
• Rare (in children -allergic to fruit juices-
• good oral hygine)
• limited to the marginal tissues and papillae
• ( Inflammation and enlargement)
• with pain +hemorrhage
• Petechiae and tendency to hematoma .
• Treatment
Vit.c in diet + water soluble vit.c (supplement) 250-500mg/day
Improve oral hygiene and Remove local irritation (plaque and
bacterial deposition)
31
34. (Acute)herpetic gingivostomatitis
• Most common viral infection
• Etiologic : Caused by Herpes simplex virus type 1
• Age: 1y<and> 5 years,
• Its peak at 3 years old
• Primary infection is asymptomatic ,
• seen in good oral hygiene kids.
• Location: mainly
• ( hard palate, attached gingiva and oral mucosa).
35. Sign and symptoms:
• Before the Oral symptoms by 1-2 days .
Extra oral symptoms:
• Cervical +sub mand. lymphadenopathy
• Fever and headache
• Generalized malaise, irritability, weakness
• and refusal to eat
• Inc. salivation skin inf. in lip
• Spread of inf. to eye& vagina
36. oral finding When fever decrease
• presence of vesicles. yellow or white liquid
• 3 to 4 mm
borders area are inflamed.
• site :all the oral mucous,
• except
• Tip of the inter dental papilla
• After a few days,
• the vesicles rupture painful ulcers,
• Ulcers heal without scarring.
10-14 days
37. Treatment
1-supportive treatment.
• Bed rest , soft diet (not hot,spicy) ,
• drink fluids I.V, fluids dehydrated , electrolyte balance
• During stage (vesicles).Child should be isolate. (infection).
• 2-palliative treatment:
• pain relief Application of mild anesthetic such as lidocaine
+ +paracetamol for fever and +orabase
• In severe case, systemic antiviral acyclovir(for 5 days).
• secondary infection of ulcers may be prevented by:
• using *chlorhexidine .mouthwash+ oxy-tetracyclin
• Vitamin supplement.
Self limit
38. recurrent herpes infection (labialis)
38
Following the primary inf.
The body make a balance between the virus and
immunity
Any upset of this balance for any reason may like:
-Cold or fever
-Dental trauma using (rubber dam)
-Sunlight
-Emotional stress
As the shape of fever cluster lip
become hemorrhagic heal with in 10 days
Treatment:
anti-viral (topical or systemic)
sunscreen
40. Acute candidiasis (thrush, candidosis)
Neonatal candidiasis,
Acute membrane c.
From mother's birth canal
clinically first 2 weeks of life
Vaginal infection
Acute candidiasis:
(White)patches
Bleeding when
remove
Chronic atrophic candidiasis:
In children
under removable orthodontic
appliances
41. Etiology:
• C. albicans ( yeast like fungus)(Monilia)
• Pathogenesis- immuno compromised
• May be after (broad spectum )antibiotic
• which allows the fungus to grows rapidly
• Painless.
Common in
• crowded areas .
• Premature ,malnourished children
41
42. Treatment:
• Stop the antibiotic use .
• Infants and very young children
• Nystatin 1ml (100,000U)
• dropped in to mouth
• for local action
• 4 times a day.-for 7-21 days
• miconazole (daktarin) gel
• (10mg/ml) 1 to 2 ml
• applied over affected areas
• 4 times a day
48. Recurrent aphthous ulcer
-Occurs between school age children.
-site: oral mucosa
• Buccal and labial mucosa tongue and gingiva
are commonly involved
• painful ulceration as single or multiple <1cm>
• Start small with burning sensation
• With in 2-3 days
• (ulceration ) increase. in size
49. Etiologic: un known but may be:
-Lesion surrounded by inflammatory cells cause:
Immunological abnormality: mucosal
destruction T-mediated immunological
reaction.
-Microbial organism (bacteria)
-Systemic factors: like nutritional deficiency
(folic acid)
Treatment
• Topical orabase –chlorhexidine mouthwash
+patch
• Nutritional diet.
• Maintenance of oral hygiene.
Self limit
51. Acute necrotizing
ulcerative gingivitis (ANUG)
Characterized by punching out
(rapid destruction )in interdental papilla
Age: in children (6-12)years
Duration: not self limiting
if not ttt Noma (cancrum oris)
in children with –low socioeconomic level
-with history of (measles or chicken pox)
ETIOLOGY:
Microbial organism
spirochetes, fusiform bacteria
52. Clinical features:
Oral:
- Single or group of teeth
(necrotic ulceration)
-Surface of gingival craters is covered by
p.membranous slough.( gray)
-If it removed bleeding
-Bad odour (halitosis)+pain+ salivation
Extra oral and systemic symptoms:
• **Submaxillary lymphadenopathy
• Fever + malaise
3-11 days
53. Treatment:
• Perform ultra sonic scaling and sub-gingival
curettage under local anaesthesia.
• Remove pseudomembrane.
• Patient counselling should include specific oral
hygiene instructions, (3%hydrogen peroxide).
• For systemic signs of systemic involvement,
• the recommended antibiotics are:
o Metronidazole, 250 mg 3 x daily for 7 days
oTopical antibiotics is contraindicated
oSurgical remove after relief of acute
symptoms
54. Recurrence may be due to:
• An immunological phenomenon.
• Persistence of gingival deformity.
• Failure to eliminate the acute symptoms.
• Patient did not complete the ttt .
54
56. • It is inflammatory disease of gingiva and
deeper tissues of periodontium
Characterized by:
• pocket formation
• destruction of supporting alveolar bone.
bitewing radiograph are often used
to clinically confirm the diagnosis.
57. 1-Chronic periodontitis
57
shows slow –moderate progression
loss of periodontal attachment and bone,
(mild -moderate –sever).
Treatment
oral hygiene instructions ,
scaling and root planning and correction of local factors
overhanging restorations and calculus .
lo
Localized
>30%
Generalized
<30%
58. 2-Aggressive periodontitis
• COMMON FEATURES defined based on the
following primary features
• Non-contributory medical history
• Rapid attachment loss and bone destruction
• Familial aggregation of cases.
59. Localized Aggressive
periodontitis(LAgP):
Clinical features:
• characterized by “sever interproximal
loss of attachment and bone around
• permanent incisors and first permanent molars”
AND may be around primary teeth.
Etiology:
• Nutrophil defect
• Anomalies of chemotaxis
• +phagocytosis +bacteria
60. Generalized aggressive
periodontitis (GAP):
• It sometimes occurs in adolescents and
teenagers.
• Characterized by generalized interproximal
attachment loss affecting
• at least three permanent teeth other than
incisor and first molar.
• Associated with heavy accumulation of
plaque and calculus.
62. A combined regimen of :
• regular Scaling and root planing and surgery
• +with systemic antibiotic
A combination of metronidazole (250 mg) &
amoxicillin (375 mg), three times a day for 8 days
Treatment:
63. 3-periodontitis associated with genetic
disorders
papillon – lefevre syndrome
Common finding:-
is severe gingival inflamation ,
early loss of deciduous teeth start at 3y to 5y
and permanent dentition .
- hyperkeratosis in
(palms of hand +soles of feet)
Treatment:
complete denture.
Contour –shape of teeth , their alignment in arch, location n size of area of proximal contact, facial & lingual gingival embrassure.
Consistency- gingiva is firm and resilient , wih exception of free marginal gingiva,tightly bound to the underlying bon.
collagenous nature of lamina propria and its contiguity with the mucoperiousteum of the alveolar bone determine the firmness of attached Stippling- Best view in dried gingiva, produced by rounded protubence n depressions in gingival surface. Papillary layer of connective tissue projects into elevation, and the elevated n depressed area are covered by strat. Squamous epi.
In some patients gingivitis proceeds to periodontitis , which is more difficult to treat. Therefore clinician must be vgilant to detect the early stage of gingivitis and carry out effective measures to prevent the progression of disease.
Younger children have less plaque, and gingiva appear to be less reactive to the same amount of plaque.
Uncommon in early primary dentition.
Orthodontic applainces r associated with incresed plaque retention and incresed bleeding on probing.
It is well-known consequence of administration of
Covering to considerable amount of crown portion.
h/f- hyperplasia of conn. Tissue and epi. Acanthosis of epi and elongated rete pages exiend deep into conn. Tissue, abundance of collagen bundles and fibroblant and formation of new BV.
Conditions can becomeextreemsymptoms covering the crowns of teeth and interfering with the eruption or occlusion.
moniliasis
Remain letent untill reactivated, HSV-1 in trigeminal ganglion, HSV-2 in lumbosacral
With varying degree of edema and gingival bleeding
So that parting of lip during speech n swallowing become extreemly painful and difficult.
Diagnosis:Rise in serum antibodies HSV-1,in cytologic study ballooning degenrtion of cells, multinucleated gaint cells, hisotpahtological finding- lipschutxz bodies. Lesion culture
Overgrowth of yeast on oral mucose leads to desquamation of epithilial cells and accumulation of bacteria, necrotic tissue.
These debris combine to form pseudomb. Which adhere closely to mucosa.
neutropenia of childhood is diagnosed between 6 and 24 months of age and is characterized by frequent and multiple pyogenic infections of the skin and mucous membranes.
IgG IgM bind to the mucosal surface
Sussequently extending to the marginal gingiva anf rarely to attached gingiva and oral mucosa.
AP is used as a generic term to describe a heterogenous grp of periodontal disease occuring in younger individual who are otherwise healthy.
AP can be viewed as 2 categories of periodontits that may have overlapping etiologies and clinical presentations.
It is also called localized juvenile periodontitis, is
characterizd by the loss of attachment and bone around the permanent incisors and first permanent molars
Attachment loss is rapid, 3 times the rate of chronic disease.
15- yr old black female pt who had atwin wid similar disease
It affect entire dentition and is not self-limiting.
Not associated with high level of AAC tht occur in LAP but istead has a microbial profile closer to that of chronic disease.
Clinical view showing minimal plaque and inflammation. A provisional wire and resin splint had been placed to stabilize the tooth.
22 Yr old black male patient with family history of early tooth loss
